BACKGROUND: It is unclear if cigarette smoking and alcohol consumption are associated with thyroid cancer risk. Our aim was to explore for any associations between cigarette smoking and alcohol consumption with thyroid cancer, after adjusting for potential confounders.
METHODS: Using data from the Korean National Health Insurance database, we retrospectively identified individuals aged ≥20 years who participated in the 2009 health screening program and were followed until 2017. We estimated the adjusted hazard ratio (aHR) for the risk of thyroid cancer using a Cox proportional hazard model, adjusted for age, sex, regular exercise, monthly income, body mass index, diabetes mellitus, and dyslipidemia.
RESULTS: During a mean follow-up period of 8.33 ± 0.57 years, of 9,699,104 participants, 89,527 (0.9%) were diagnosed with thyroid cancer. Compared with those who never smoked, current smokers had a lower risk of thyroid cancer (aHR: 0.74, 95% confidence interval [CI]: 0.72-0.76), while ex-smokers did not (aHR: 0.98, 95% CI: 0.96-1.01). There was no significant dose-response relationship with regard to daily amount smoked, duration of smoking, or pack-years. A reduced risk of thyroid cancer was observed in subjects who reported the following categories of alcohol intake (compared with none): mild (aHR: 0.92, 95% CI: 0.90-0.93), moderate (aHR: 0.86, 95% CI: 0.84-0.89), and heavy (aHR: 0.86, 95% CI: 0.82-0.89). Inverse associations with thyroid cancer risk were observed regarding the number of drinking episodes per week and the number of drinks per occasion. A submultiplicative effect of smoking and alcohol consumption was observed (p-interaction <0.001).
CONCLUSIONS: We observed that thyroid cancer risk was inversely associated with smoking and alcohol consumption, with a significant interaction between these variables.
BACKGROUND: Alcohol consumption potentially influences psychological well-being in beneficial and harmful ways, but prospective studies on the association show mixed results. Our main purpose was to examine prospective associations between alcohol consumption and psychological well-being in middle-aged men and women.
METHODS: The study sample included 4148 middle-aged individuals (80% men) from the Copenhagen Aging and Midlife Biobank who reported their alcohol consumption (average weekly consumption and frequency of binge drinking) at baseline in 2004 or 2006 and reported their psychological well-being (satisfaction with life and vitality) at follow-up in 2009-2011. Analyses were adjusted for sociodemographic factors, lifestyle, social relations, and morbidity.
RESULTS: For satisfaction with life at follow-up, lower scores were observed in men and women who were alcohol abstinent at baseline as well as in men with heavy alcohol consumption compared with moderate alcohol consumption at baseline. Moreover, men with weekly binge drinking at baseline had lower satisfaction with life scores at follow-up than men with moderate frequency of binge drinking (1-3 times/month). In relation to vitality at follow-up, alcohol abstinence at baseline in men and women and heavy alcohol consumption at baseline in men were associated with lower scores compared with moderate alcohol consumption (yet in men these findings were not robust to adjustment for covariates).
CONCLUSIONS: Alcohol abstinence seems to be prospectively associated with adverse psychological well-being (vitality and life satisfaction) in men and women, while heavy alcohol consumption seems to be prospectively associated with adverse satisfaction with life in men. Finally, a prospective association between weekly binge drinking and lower life satisfaction was observed in men.
BACKGROUND: Epilepsy is one of the most common neurological disorders, affecting approximately 50 million people worldwide. Although a positive association between alcohol consumption and epilepsy has been demonstrated in previous meta-analyses of case-control studies, the results of several recently published large cohort studies are contradictory. Therefore, we conducted an updated meta-analysis that included more recent data to clarify the association between alcohol consumption and epilepsy.
METHODS: The search was performed on 25 January 2021 using the Embase and MEDLINE databases. Cohort or case-control studies were eligible for inclusion in this study. We used restricted cubic spline analysis to perform a dose-response meta-analysis.
RESULTS: A total of eight studies, including three cohort and five case-control studies, were included in our meta-analysis. The pooled risk of epilepsy was 1.70 (1.16-2.49) in alcohol users compared to non-drinkers. Subgroup analysis of 50 g units showed that the epilepsy risk increased as alcohol intake increased. The pooled risk of cohort studies was 1.00 (0.65-1.54), and the pooled risk of case-control studies was 2.61 (1.29-5.29). According to the dose-response analysis, the regression coefficient was 1.009 (1.004-1.014), indicating a significant positive dose-response relationship.
CONCLUSION: Unlike the case-control studies, the cohort studies did not reveal a significant association between alcohol consumption and epilepsy. Further large cohort studies for the general population are required to assert a definite causal relationship between alcohol consumption and epilepsy and to identify a potential threshold.
PURPOSE OF REVIEW: A clear link between excessive alcohol consumption and cardiovascular disease (CVD) has been established, but no consensus exists on the effects of moderate alcohol consumption on CVD.
RECENT FINDINGS: A lower risk of coronary heart disease and myocardial infarction among moderate drinkers compared to abstainers has been consistently observed in epidemiological studies and meta-analyses of these studies. However, ambiguity remains on the effect of alcohol on other CVDs and all-cause mortality. Short-term randomized controlled trials (RCT) have identified potentially beneficial effects of alcohol consumption on cardiovascular risk factors, but studies investigating genetic polymorphisms that influence alcohol consumption (i.e., Mendelian randomization) have yielded inconclusive results.
To date, a long-term RCT providing causal evidence is lacking but urgently needed. Triangulation of evidence from different study designs, including long-term RCTs, pragmatic trials and the evaluation of policy measures, combined will lead to the best available evidence.